The neurotoxicity of parathion-induced acetylcholinesterase inhibition in neonatal rats.
The biochemical and morphological effects of postnatal acetylcholinesterase (AChE) inhibition were examined in rat pups dosed with paration, at time points critical to hippocampal neurogenesis and synaptogenesis (i.e., day 5-20). In treated pups, sacrificed on day 21, hippocampal histopathology, as assessed by light and electron microscopy, consisted of cellular disruption and necrosis in the dentate gyrus (DG), and CA4 regions. Synaptic disruption in the DG molecular layer was suggested by histochemical preparation using both the Timm's and AChE stains. In parathion-treated pups, sampled at day 12, hippocampal AChE was depressed 73% and [3H] quinuclidiny benzilate (QNB) binding was depressed by 36%. The above results indicate that morphological and biochemical consequences are associated with persistent AChE depression in neonatal rats.
Veronesi
B
B
U.S. Environmental Protection Agency, Neurotoxicology Division MD74-B, Research Triangle Park, North Carolina 27711.
Pope
C
C
D000110:Acetylcholinesterase / Q000378:metabolism; D000818:Animals; D000831:Animals, Newborn; D002800:Cholinesterase Inhibitors / Q000633:toxicity*; D005260:Female; D006624:Hippocampus / Q000187:drug effects / Q000473:pathology / Q000648:ultrastructure; D008297:Male; D008854:Microscopy, Electron; D009336:Necrosis / Q000139:chemically induced; D009420:Nervous System / Q000187:drug effects*; D010278:Parathion / Q000633:toxicity*; D051381:Rats
D002800:Cholinesterase Inhibitors; D010278:Parathion; D000110:Acetylcholinesterase